Chapter 5 94 Abstract Objective Increasing magnesium intake might reduce the risk of cardiovascular disease (CVD). Whether potential effectsoncortisol contribute to thesebeneficial effectsoncardiovascular health remains unclear. We therefore studied effects of long-term oral magnesium supplementation on glucocorticoid metabolism, specifically on the excretion of urinary cortisol, cortisone, and their metabolites, as well as on the ratios reflecting enzymatic activity of 11β-hydroxysteroid dehydrogenases (11β-HSDs) and A-ring reductases. Design A post-hoc analysis of a randomized trial with allocation to a magnesium supplement (350 mg/d) or a placebo for 24-wk. Patients Forty-nine overweight men and women, aged between 45-70 years. Measurements Cortisol, cortisone, and their metabolites (tetrahydrocortisol [THF], allo-tetrahydrocortisol [allo-THF], and tetrahydrocortisone [THE]) were measured in 24-h urine samples. Enzymatic activities of 11β-HSD overall and of 11β-HSD type 2 were estimated as the urinary (THF + allo-THF [THFs])/THE and cortisol/cortisone ratios, respectively. A-ring reductase activity was assessed by ratios of THF/allo-THF, allo-THF/cortisol, THF/cortisol, and THE/cortisone. Results After 24-wk, urinary cortisol excretion was decreased in the magnesium group as compared with the placebo group (-32 nmol/24-h, 95% CI: -59; -5 nmol/24-h, P=0.021). Ratios of THFs/THE and cortisol/cortisone were decreased following magnesium supplementation by 0.09 (95% CI: 0.02; 0.17, P=0.018) and 0.10 (95% CI: 0.03; 0.17P=0.005), respectively. No effects were observed on A-ring reductase activity. Conclusions We observed a beneficial effect of magnesium supplementation towards a lower 24-h urinary cortisol excretion together with an increased activity of 11β-HSD type 2. Our findings may provide another potential mechanism by which increased magnesium intake lowers CVD risk (ClinicalTrials.gov identifier: NCT02235805).
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